Assessment and Management of Kidney Failure
Acute kidney injury (AKI) should be classified using the RIFLE or KDIGO staging systems based on serum creatinine changes and urine output, while chronic kidney disease (CKD) requires confirmation of kidney damage or reduced eGFR persisting ≥3 months, with both conditions demanding immediate assessment of reversible causes and risk stratification to guide management intensity. 1
Acute Kidney Injury Assessment
Diagnosis and Staging
Use the RIFLE classification system to stage AKI severity: Risk (serum creatinine increase 1.5× baseline or urine output <0.5 ml/kg/h for 6 hours), Injury (creatinine 2× baseline or urine output <0.5 ml/kg/h for 12 hours), and Failure (creatinine 3× baseline or >4.0 mg/dl with acute rise ≥0.5 mg/dl, or urine output <0.3 ml/kg/h for 24 hours) 1.
Distinguish AKI from acute kidney disease (AKD): AKI represents the initial 7 days of injury, while AKD extends from 7 days to 3 months, recognizing that kidney dysfunction may not resolve quickly and requires ongoing monitoring 1.
Calculate baseline creatinine when unknown using the simplified MDRD formula assuming a normal GFR of 75-100 ml/min per 1.73 m², adjusting for age, race, and sex 1.
Immediate Management Priorities
Discontinue all nephrotoxic agents immediately including NSAIDs, aminoglycosides, and contrast media when AKI is identified 1, 2.
Ensure adequate volume status and perfusion pressure through fluid resuscitation in pre-renal AKI, as volume depletion is the most common and modifiable risk factor 1, 3, 2.
Monitor serum creatinine and urine output continuously during the acute phase to track progression and response to interventions 1.
Perform renal ultrasound urgently to exclude obstructive uropathy, which requires immediate urologic decompression via nephrostomy or ureteral stent 4.
Indications for Renal Replacement Therapy
Initiate urgent dialysis for life-threatening complications: severe hyperkalemia unresponsive to medical management, volume overload with pulmonary edema, uremic symptoms (pericarditis, encephalopathy), or severe metabolic acidosis 1, 4, 3.
Timing of KRT initiation remains controversial with no consistent benefit demonstrated for early-start dialysis in the absence of absolute indications 2.
Follow-Up After AKI
Evaluate all AKI survivors at 3 months to assess for resolution, new-onset CKD, or worsening of pre-existing CKD 1.
Intensity of follow-up should be proportionate to AKI severity: Stage 3 AKI, non-recovery, or pre-existing CKD warrant nephrology referral and more frequent monitoring (every 1-3 months initially) 1.
Measure both serum creatinine and UACR at follow-up as AKI survivors have substantially increased risk of developing CKD, hypertension, and cardiovascular disease 1, 5.
Chronic Kidney Disease Assessment
Diagnosis and Confirmation
Test using both eGFR and UACR simultaneously on all at-risk patients, as CKD can be diagnosed by either abnormality and both provide independent prognostic information 1, 6.
Confirm chronicity by demonstrating persistence ≥3 months through review of historical measurements, repeat testing, imaging showing reduced kidney size or cortical thinning, or medical history of conditions causing CKD 1.
Do not assume chronicity from a single abnormal result as this could represent recent AKI or AKD rather than CKD 1.
Use eGFRcr-cys (combined creatinine and cystatin C) when available for more accurate GFR estimation in clinical situations where eGFRcr alone is less reliable 1.
Risk-Based Screening
Screen immediately in all adults with: diabetes mellitus, hypertension, age >60 years, family history of kidney disease, cardiovascular disease, or obesity 6, 5.
Do not perform routine screening in asymptomatic adults without risk factors as the risk of false positives and potential medication harms outweigh benefits in low-risk populations 6.
Determining Underlying Cause
Establish etiology systematically using clinical context, personal and family history, medications, physical examination, laboratory measures (including hepatitis B/C serologies, autoimmune panel with complement levels, ANCA, anti-GBM antibodies), imaging, and genetic testing when indicated 1, 6.
Consider kidney biopsy when: the underlying cause is uncertain, atypical features suggest non-diabetic kidney disease in diabetic patients (absence of retinopathy, short disease duration, rapid decline, active sediment), nephrotic syndrome is present, or there is rapidly progressive kidney function loss 1, 6.
CKD Management by Stage
CKD Stage 1-2 (eGFR ≥60 ml/min/1.73 m²)
Confirm kidney damage is present by measuring UACR, as these stages require evidence of damage (UACR ≥30 mg/g, hematuria, or structural abnormalities) in addition to normal or mildly decreased GFR 6.
Target blood pressure <130/80 mmHg in all CKD patients regardless of stage 6.
Initiate ACE inhibitor or ARB for patients with UACR 30-299 mg/g and hypertension, or UACR ≥300 mg/g regardless of blood pressure 6.
Start statin therapy for cardiovascular risk reduction, as CKD patients have 5-10 times higher cardiovascular mortality risk 6.
Monitor annually if UACR <30 mg/g, increase to twice yearly if UACR 30-300 mg/g, and 3-4 times yearly if UACR >300 mg/g 6, 5.
CKD Stage 3a (eGFR 45-59 ml/min/1.73 m²)
Measure UACR immediately to complete risk stratification, as the combination of eGFR and albuminuria determines progression risk and monitoring intensity 6, 5.
Screen for CKD complications: complete metabolic panel (electrolytes, bicarbonate), hemoglobin, calcium, phosphate, intact PTH, and 25-hydroxyvitamin D 6.
Monitor every 6-12 months depending on albuminuria category and rate of eGFR decline 5.
CKD Stage 3b (eGFR 30-44 ml/min/1.73 m²)
Review historical eGFR measurements to confirm chronicity and calculate rate of decline 6.
Perform comprehensive laboratory evaluation: complete metabolic panel, CBC, calcium, phosphate, PTH, 25-hydroxyvitamin D, and UACR 6.
Identify nephrotoxic exposures including NSAIDs, lithium, calcineurin inhibitors, and aminoglycosides 6.
Monitor potassium closely especially when initiating RAS inhibitors or mineralocorticoid receptor antagonists, rechecking within 2-4 weeks of medication changes 6.
Adjust monitoring frequency based on risk: moderate risk (UACR <30 mg/g) twice yearly, high risk (UACR 30-300 mg/g) three times yearly, very high risk (UACR >300 mg/g) four times yearly with nephrology referral 6.
CKD Stage 4-5 (eGFR <30 ml/min/1.73 m²)
Refer to nephrology immediately as this threshold indicates high risk for progression to end-stage kidney disease and need for preparation for kidney replacement therapy 1, 6.
Monitor electrolytes closely particularly potassium and phosphorus, as Stage 5 carries risk of life-threatening hyperkalemia 4.
Avoid subclavian catheters if possible to preserve future vascular access options 1.
Nephrology Referral Indications
- Mandatory referral criteria: eGFR <30 ml/min/1.73 m², UACR ≥300 mg/g with continuously increasing albuminuria despite optimal therapy, eGFR decline >5 ml/min/1.73 m² per year, uncertain etiology or atypical features, difficulty managing CKD complications (anemia, mineral-bone disorder, resistant hypertension, hyperkalemia), or consideration of kidney biopsy 1, 6.
Common Pitfalls to Avoid
Never rely on serum creatinine alone—always calculate eGFR using validated equations (CKD-EPI 2021) and measure UACR, as both provide independent prognostic information 1, 6.
Do not discontinue ACE inhibitors or ARBs for minor creatinine increases (<30%) in the absence of volume depletion, as these medications provide long-term kidney and cardiovascular protection 6.
Never combine ACE inhibitors with ARBs as this increases adverse events without additional benefit 6.
Avoid testing UACR during urinary tract infection as this causes false positive results for proteinuria 5.
Do not assume normal-sized kidneys exclude advanced CKD, particularly in diabetic nephropathy and infiltrative disorders where kidney size may be preserved despite significant dysfunction 6.